Symposium on Clinical Toxicology for the Small Animal Practitioner

Clinical Toxicities of Domestic and Wild Caged Birds Bernard F. Feldman, D.V.M.,* and Samuel M. Kruckenberg, D.V.M., Ph.D. t

This article examines a neglected field in avian medicine: individual care of the caged bird affected by toxin. Where possible discussion includes sources of toxins, signs, treatment, secondary effects, and diagnostic methodology. Two categories of caged birds are discussed. The first section, domestic birds, deals primarily with the Psittaformes (lories, lorikeets, cockatoos, budgerigars or parakeets, macaws, parrots, conures, and lovebirds) and the Passeriformes (canaries, finches, mynahs, and crows). The second section, wild birds, includes the Falconiformes (hawks, eagles, owls, falcons, ospreys), Anseriformes (geese, ducks, and swans), Columbiformes (doves and pigeons), and a few miscellaneous species. Of necessity the discussion on any particular area is brief. The reader is referred to the selected readings at the conclusion of this article for a more in-depth examination.

CLINICAL TOXICITIES OF DOMESTIC CAGED BIRDS This discussion focuses on known and potential toxicologic hazards. Several anatomic and physiologic facts are worth mentioning. The respiratory system of birds is different from that of mammals. In mammals the alveoli are located at the end of the bronchial tree, however in birds they are located at the site of the parabronchi. Most inspired air does not go directly to gas-exchanging alveoli but comes first to the air sacs. From there, during expiration, it goes to the respiratory tissue by way of the parabronchi. Anthracosis of the lungs in pet *Instructor, Department of Infectious Diseases, Resident in Clinical Pathology, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas tAssistant Professor, Department of Pathology, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas Veterinary Clinics of North America- Vol. 5, No. 4, November 1975

653

654

BERNARD F. FELDMAN, SAMUEL

M.

KRUCKENBERG

birds is a very common condition and is not considered to be pathologic.12 The avian kidney differs from its mammalian counterpart in anatomy as well as in physiology. Like the liver, the kidney is constructed of lobules with a central vein and is supported by arterial and portal blood. The glomerulae are small and their filtration capacity is remarkably lower than in mammals. Activities of the tubules, on the other hand, are much higher than in mammals. The end product of protein metabolism is uric acid which is excreted mainly by the tubules. During passage of the primary urine through the tubules, it becomes a colloidal supersaturated solution of urates because of resorption of water and bases (resulting in a lowering of the pH), until finally uric acid crystals are precipitated. In the process uric acid loses its osmotic activity and water can be iso-osmotically resorbed. This mechanism enables the bird to excrete waste products and at the same time save water. Filtration as well as resorption, is not necessary to the same extent as in mammals. The filtration-resorption system of mammals does not exist in birds as the tubular apparatus is functionally much superior to the glomerular apparatus. 12 The urate tubular excretion mechanism is not yet known in its entirety, but it is known several other substances are excreted, at least partly, by this same mechanism. This is particularly true of sulfonamides. The renal-portal system, also called the vena renales adve~ hentes, is supported with blood from the v. iliaca externa, v. hypogastrica, and v. coccygico-mesenterica. By this means it is possible for blood from the caudai parts of the intestines containing many absorbed substances to pass to the kidneys without being previously filtered by a lymph organ or the liver. Nephrotoxic substances from the intestines, therefore, can act directly on avian kidneys; the portal blood supply serves only the tubular part of the kidneys. The glomerulae, as a rule, are not involved in the pathologic processes of the kidney. Although impressive by histological examination, damage of the tubular system often shows no obvious clinical signs, and probably there is a much higher spontaneous recovery rate than in mammals. 12 Metabolic activity is high in birds. Blood sugar is about 200 mg per cent in normal animals, therefore sudden death by starvation may occur more often than in mammals. Birds that do not eat by themselves must be fed by hand or injected with nutrient solutionsP Endogenous Intoxication

Endogenous intoxication or autointoxication, the absorption of waste products due to inappropriate feeding, is a common clinical complaint in avian practice. It is imperative the clinician be familiar with correct feeding practices and species-specific diets. Diets can be quite diverse in apparently closely related species. Several excellent

ToxiCITIES oF DoMESTic AND WILD CAGED BIRDS

655

sources of information on food requirements of birds are available. 27 • 28 Signs of endogenous intoxication are those of digestive disturbance. Vomiting, anorexia, emaciation, salivation, diarrhea (watery stools), pasting of the vent, straining, impacted crop, and enlarging abdomen are among those signs most often seen. It is important to distinguish physiologic regurgitation due to courting and mating, a mirror, or the owner, from pathologic regurgitation. The latter exhibits pasted feathers in a ring around the head from flinging vomitus. Common sources of endogenous intoxication will be spoiled seeds, fruits or greens, or bacterial infections such as Salmonella spp., Pasteurella spp., or Escherichia coli. It should be noted that gram-negative organisms are not normal flora of Psittaformes and other grain and seed eating birds. Hence, any of these organisms, including E. coli, should be considered significant. Other sources of endogenous intoxication are poor or inadequate grit, lack of fresh foods and fresh clear water, or removal of the young from parents before they can husk their own seeds. Omnivores do have E. coli in the gut. Some granivores eat insects at certain times of the year and at that time may normally have E. coli present. Thorough clinical history and physical examination are requisite before toxins may be implicated. Direct smears of droppings, or exudates, or both, may reveal bacteria, fungi, parasites, or trichomonads. Culture may be informative. Any stasis of intestinal contents could result in endogenous intoxication. Because medicating birds via feed and water is unpredictable at best, direct, oral, or injectable routes are preferred (see section on Therapeutic Drug Intoxication). Palliative measures inlcude a few drops of olive oil to relieve constipation, Kaopectate* for diarrhea given at a dose of two drops initially and one drop four times daily for several days thereafter, and specific drug therapy.

Fungal and Other Food Toxins Under present day harvest methods, storage fungi are a great problem and are associated with livestock poisonings. One species, Aspergillus flavus, grows on moldy corn, other grains, and peanuts and produces a toxin known as aflatoxin. Birds may be affected acutely, subacutely, or chronically. Acute signs include anorexia, ataxia, and depression. Often death can occur with no clinical signs having been observed. Aflatoxin, a highly substituted coumarin, causes bile duct proliferation and hepatic parenchymal necrosis. It is considered to be a potent hepatocarcinogen. There is no specific treatment for aflatoxicosis. Avoidance of stress, adequate dietary protein, and lipotropic agents are helpful. 3 In our practice, breaking a capsule of a lipotropic agent and sprinkling the feed has been helpful in a wide variety of die*The Upjohn Company, Kalamazoo, Michigan.

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BERNARD F. FELDMAN, SAMUEL

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KRUCKENBERG

tarily induced hepatic problems. It is one of the few medications we use on food. Cardiac zygomycosis (phycomycosis) has been reported in budgerigars.2 Birds died suddenly having presented nonspecific signs. On postmortem examination diffuse small foci of myolysis and hemorrhages were seen throughout the myocardium. Walls of cardiac blood vessels were infiltrated with hyphae and their lumens were obstructed by thrombi which were also colonized by fungal elements. Food sources are suspected. Alcoholic intoxication is common in free-flying domestic birds. The practice of drinking alcoholic beverages is often encouraged by misguided but well meaning owners. Clinical signs are depression, sitting with closed eyes, regurgitation, and loose droppings. Supportive therapy should be instituted and should include moist warmth (80 to 85° F.) and fluids when indicated. Five per cent dextrose in saline (0.2 to 0.25 ml) may be administered subcutaneously in the wing web or the loose skin of the neck. Salt poisoning can occur when birds ingest excessive amounts of sodium chloride. Sources include mineral blocks, high salt content chick mashes, and pickling brines. Loss of appetite, somnolence, enteritis, thirst, dyspnea (due to lung edema), opisthotonos, convulsions, and inability to stand are signs. Histopathologic examination demonstrates degenerative changes in heart, liver, and kidneys. Supportive treatment is suggested. Available fresh water and a salt-free diet are important to affected birds. Atheromatosis particularly of the brachiocephalic aorta is easily produced by adding c~olesterol to ordinary dietary seeds. 15 The veterinary clinician would be well advised to have knowledge of high fat content and high cholesterol content foodstuffs. 27 Clinically, fatty enlargement of the liver is a common finding. Dietary correction often produces positive results. In an experiment to determine carcinogenesis in different animal species in response to injection of diethylnitrosamine (DEN A) parakeets developed hepatocarcinomas. 31 These birds received intramuscular injections of DENA totaling 70 mg per kg weekly for a total dose of 2,800 mg per kg ± 400 mg per kg. It is noteworthy that all animals tested in this experiment developed hepatic tumors. Nitrosamine could occur naturally in the gut if nitrates or nitrites ingested met an acidic environment. This is a substance that occurs naturally in some plants. Rodenticides and Metals Strychnine saturated, plain canary seed has been used to poison mice. 27 This is a readily available and attractive source of food for domestic birds. Clinical signs are tetanic spasms, paralysis, and respiratory failure. Strychnine is readily absorbed from the digestive tract and

ToxiCITIES OF DoMESTIC AND WILD CAGED BIRDS

657

has a cumulative action. The use of methocarbamol (Robaxin) at a dosage of 67 mg per pound to effect has occasionally been effective in early forms of known poisonings. The authors readily admit that their success ratio is low. Prevention is the best remedy. Arsenic is used in ant poisons, herbicides, insecticides, drugs, paints, food additives, and mouse and rat baits. Clinical signs include ruffled feathers, drooping wings, anorexia, regurgitation, and ataxia. Supportive treatment is mandatory as has previously been described. Fluid therapy is recommended (see section on Therapeutic Drug Intoxication). The use of British anti-lewisites (BAL, dimercaprol) at 2 mg per pound and sodium thiosulfate have been recommended for poultry after absorption of arsenicals has taken place. 32 Lead salts are present in insecticides, linoleum, golf balls, paint, lead weights, putty, ceramics, and poorly glazed china. 40 A conure presented to our clinic had chewed several lead curtain weights. This patient had watery droppings. The particles were radiographically demonstrable in the gizzard. Several erythrocytes were stippled, enucleated, or teardrop shaped. CaEDT A was administered, 27 mg per kg daily subcutaneously, adjusted for the patient's weight. The dosage was diluted and this was divided into three equal doses. This regimen was followed for 72 hours when all particles had been passed. The patient made an uneventful recovery. It should be noted that lead can affect the nervous system producing ataxia and paralysis of extensor muscles. Insecticides and Herbicides Lead compounds and arsenic compounds are used as insecticides and herbicides. Nicotine sulfate, the toxic alkaloid of tobacco caused severe losses in a budgerigar aviary. The substance found in Blackleaf 40 was used to control insects. Deaths were acute. In some cases death was preceded by convulsions. In poultry, dilation of the pupil and ecchymoses in lungs, liver, and heart are seen on postmortem examination. No treatment has been described but the use of stimulants has been suggested. Birds affected by household spray insecticides containing chlorinated hydrocarbons became ill about 48 hours after initial usage. These birds became listless, anorectic, ataxic, and demonstrated erratic flight. Several actually died while in flight. Nervous signs such as side-to-side head movements, head tremors, and eyelid blinking were noted. Diagnosis was made from clinical signs and from analysis of carcass fats. Postmortem lesions included pectoral muscle ,atrophy and congested internal organs. If a known insecticide bait has been ingested, immediate evacuation of the crop is necessary. Organic phosphorus compounds have also been found to cause muscle tremors. Congestion of the lungs has been found on postmortem examination. Though no specific therapy has been suggested for domes-

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BERNARD F. FELDMAN, SAMUEL

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KRUCKENBERG

tic caged birds, repeated injections of atropine at 0.1 to 0.2 mg per kg subcutaneously or intramuscularly and 2-P AM (Protopam chloride) are recommended for poultry. It must be remembered that 2-P AM is contraindicated for carbamate poisoning. The dosage of 2-P AM in dogs is 10 to 100 mg per kg. We have not had any personal experience with this drug in birds. Therapeutic Drug Intoxication

Medications appropriate for parenteral treatment of caged birds using correct dosages based on weight and physical condition are recommended (Table 1). 21 A microliter syringe delivery system is also recommended. It is our practice to experimentally inject hospital birds with unfamiliar drugs prior to using them therapeutically on patients. The number of drugs offered for all kinds of conditions are numerous. Pet birds are generally sensitive not only to the side effects of the drugs, but also to the diluents used to make a drug injectable, or to the component that makes it water soluble. Tissue damage and necrosis after i~ection are seen frequently. Sometimes signs such as trembling and other central nervous disorders, nausea with regurgitation and tears, imbalance, and increased respiratory rate are seen shortly following injection. These signs are similar to hypersensitive reactions or shock and in some instances can be followed by death in a few minutes post injection. These signs are most likely not a true hypersensitive reaction since they are almost always seen immediately after the first treatment. 12 Drugs should be diluted, but the total volume for intramuscular injection for a budgerigar or a canary should not exceed 0.05 ml. In addition, 0.05 ml of a commercial Vitamin B and C mixture should be administered to treat against a possible subclinical hypovitaminosis which may become more severe during antibiotic therapy. 12 Topical medication should also be used with care. Toxic topical medications should be avoided as birds will pick at and ingest the preparations. Drugs contraindicated in birds are procaine (in solution greater than 0.25 per cent), Xylocaine (lignocaine hydrochloride), procaine penicillin, DDT, streptomycin and dihydrostreptomycin in excess of 1 mg per 20 mg of body weight, methocaine, and epinephrine. Since Psittaformes normally have only gram-positive enteric flora, gram-positive bacteriostatic or bactericidal drugs should be used with extreme caution. When this type of drug is indicated use low dosages and do not prolong therapy. Lactinex tablets* (Lactobacillus acidophilus) reestablish gut flora. One tablet is crushed on seed daily for several days. *Hynson, Westcott and Dunning, Inc., Baltimore, Maryland.

ToxiCITIES OF DoMESTic AND WILD CAGED BIRDs

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Antimicrobial Drugs Erythromycin (Schering, Eli Lilly) as erythromycin-glucohepatonate intravenous injection (0.05 mg per gm intramuscularly, or orally) will have little or no tissue reaction as compared with other preparations of erythromycin. Chloramphenicol (Parke-Davis) water soluble solution for oral administration is satisfactory. The same substance from the same company in the intramuscular preparation has caused severe local tissue reactions. Injectable tylocine (Eli Lilly) should be used with caution because of the possibility of major local tissue reactions. Streptomycin may cause death in members of the psittacine family. It seems to cause acute shock. In passerine birds it is not free of side effects although appears to be of some value in Falconiformes and Anseriformes. Aureomycin administered intramuscularly may cause major local tissue reactions. Sulfa drugs are generally not recommended because of their interference with the urate excretion mechanism of the kidney tubules. In coccidiosis and some enteric bacterial infections32 they are useful and should be given orally in the insoluble form (e.g., sulfaguanidine).

Anesthetic Agents Recommendations for avian anesthetic requirements have been made.L 34 Pre-anesthetic evaluation is requisite for successful anesthesia. Nontoxic anesthetics may be lethal when administered to an avian patient in poor physical status. Local anesthetics may be used. A 0.25 per cent procaine solution has been used successfully in parakeets. 1 At higher concentrations procaine may be toxic, producing ataxia, seizures, and finally death. The use of chloroform cannot be recommended. It is a hazardous drug at best. With the advent of modern inhalation anesthetics chloroform does not belong in the avian anesthetic armamentarium. Ether, besides being a potential fire hazard, is highly irritating to mucous membranes. Control of ether dosage is difficult in birds because of differences in lung and air sac physiology. The cyclohexamines (phencyclidine, tiletamine, ketamine, etc.) when given in excessive doses may produce tremors and convulsions. 1 As with other anesthetics, the exact dosage of cyclohexamine must be calculated and the dosage reduced for debilitated birds. In our experience, recovery varies directly in relationship to the duration of anesthesia. It has also been our experience with prolonged avian inhalation anesthesia that success is dependent on the position of the surgical patient. Birds kept on their sides or too assiduously restrained often have prolonged recovery times or will die. Birds should be repositioned every 10 to 15 minutes.

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Table 1. Medications Appropriate for Parenteral Treatrnent of Cage Birds*

t:;C

M

~

SUGGESTED DOSAGE DRUG

STRENGTH

MANUFACTURER

vol./gm. body Weight

vol./30-gm. Parakeet

z

> ~

u

.., ~

Vitamins and Amino Acid Preparations I 00 fLg./ml. B 12 Bejectal and vitamin C Vitamin A 100,000 units/mi. Vi-Syneral Vitamin C Synkavite Injacom with vitamin D 3 Antibiotics and S ulfonamides Chloromycetin Succinate Tylocine Bactrovet Symbio Erythromycin

100 mg./mi. 5 mg./mi. As supplied

U.S.P. Abbott Lab. U.S.P. U.S. Vitamin & Pharmaceutical Corp. U.S.P. Roche Lab. Roche Lab.

0.0002-0.0067 mi. 0.00017-0.00034 mi. 0.00034 mi. 0.00017-0.00034 mi.

0.006-0.1 mi. 0.005-0.01 mi. 0.01 mi. 0.005-0.01 mi.

0.00034 mi.

0.01 mi. 0.01 mi. 0.01-0.03 mi.

0.00034 mi.

M t"'

u s:: >

.z

[/)

> s::

c:M t"'

~

:;.::: 100 50 100 80 50

mg./mi. mg./mi. mg./mi. mg./mi. mg./mi.

Parke Davis & Co. Corvel, Inc. Pitman-Moore Co. Warren-Teed Co. Abbott Lab.

0.00034-0.0005 mi. 0.00034-0.00068 mi. 0.00024 mi. 0.00034-0.00068 mi. 0.00009 mi.

0.01-0.015 mi. 0.01-0.02 mi. 0.007 mi. 0.01-0.02 mi. 0.005-0.01 mi.

~

c:

("l ~

M

zo:; M

~

Cl

Penicillin G, potassium Spectinomycin Lincocin Gentocin

Diluted 500,000 units/mi. 100 mg./mi. 100 mg./mi. 50 mg./mi.

0.00034-0.00068 mi. Diamond Labs. Upjohn Schering Corp.

0.00034-0.00068 mi. 0.00034-0.00068 ml. 0.00034 mi.

0.01-0.02 mi. (5000-10,000 units) 0.01-0.02 mi. 0.01-0.02 ml. 0.01 mi.

,..., 0

~

('i ::]

;; C/l

0

"1

v

Hormones

Stilbestrol Testosterone Azium ACTH Winstrol V Vetalog

25 25 1 40 50 2

mg./mi. mg./mi. mg./mi. units/mi. mg./mi. mg./mi.

U.S.P. U.S.P. Schering Corp. Armour Corp. Winthrop Lab. Squibb

0.0001-0.00034 mi. 0.00034 ml. 0.0002-0.00068 rnl. 0.00034-0.00068 ml.

0.003-01. rnl. 0.01 ml. 0.006-0.02 mi. 0.001-0.02 mi. 0.01-0.03 mi. 0.005-0.01 mi.

s::t>j

...,C/l ('i

> z tl

~

p

Miscellaneous

Nembutal Equi-Thesin Jenotone Saline and 5% dextrose Sodium iodide

0

60 mg./mi. As supplied 25 mg./mi.

Abbott Lab. Jensen-Salsbery Lab., Inc. Jensen-Salsbergy Lab., Inc.

20% solution

U.S.P.

0.00083 rnl. 0.0022-0.0025 rnl. 0.0004 mi.

0

0.025 ml. 0.066 ml. 0.012 mi.

CJ

0.01-0.03 mi.

;;

>

C'l t>j

0

td

0

*From Lafeber, T. J.: Physical examination, laboratory and medication techniques and hospitalization procedures for the common parakeet and canary. In Kirk, R. W. (ed.): Current Veterinary Therapy V. Philadelphia, W. B. Saunders Co., 1974, p. 536 with permission.

C/l

~ .....

662

BERNARD F. FELDMAN, SAMUEL

M.

KRUCKENBERG

Miscellaneous Household Hazards In homes where free-flying domestic birds have access to tobacco, cigarettes, and cigarette butts, consumption of these products leads to nicotine intoxication. Depression, prostration, and death occurs in short time periods27 (see section on Insecticides and Herbicides). Any comment on toxicities of common house plants must be naive in this era of increased interest in these plants. Philodendron is the plant most often incriminated. While the literature has made occasional mention of signs referable to central nervous system disorders in cats and dogs, we have not seen toxicity directly attributable to this plant in birds. The ivies, philodendron, and dieffenbachia cause irritation to mucous membranes, copious salivation, dyspnea, dysphagia, debilitation, and listlessness. There is no specific treatment and general supportive measures should be instituted. Other potentially dangerous ornamental plants have been described. 18 Cherry seeds contain cyanogenetic glycosides which release cyanide on digestion. They are only dangerous if the seed capsule is broken, something within the capability of the larger psittacines. The principal manifestation of cherry seed poisoning will be acute signs: rapid respirations, convulsions, and coma. Blue-green algae toxin obtained from drinking water in in-house ponds and fish tanks will cause vomiting, muscular tremors, convulsions, prostration, paralysis, and death. Onset is rapid, often within several hours, and there is no known treatment. Many household cau~tics such as lye, silver nitrate (especially when ingested while being used for hemostasis), disinfectant aerosols, ammonia, and phenolic compounds are potentially hazardous to birds. Sources are cleaning preparations, styptic pencils, and grease dissolvents. Signs are external skin maceration or mucous membrane damage and blood-flecked vomitus. Treatment consists of flushing with copious amounts of water, neutralizing with vinegar or acetic acid and olive oil or egg white as demulcents. Carbon monoxide poisoning has been reported as a cause of sudden death. Defective exhaust systems in homes, garages, and automobiles have been incriminated. Birds kept near gas stoves and heaters have been known to succumb from the fumes. Diagnosis may be made from history of exposure, muscular tremors, and cherry red blood. Treatment consists of oxygen resuscitation and administration of intravenous 50 per cent glucose, 1 ml per pound. The accidental death of pet birds exposed to gaseous decomposition products of overheated cooking pans lined with polytetrafluorethylene (PTFR) was reproduced experimentally by heating dry PTFRlined pans to temperatures slightly above 500° C. 7 In contrast to small mammals (guinea pigs, mice) which remained healthy under conditions of the experiment, small birds died of toxic volatile products after 20 to

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663

30 minutes showing signs of acute lung edema and liver dystrophy. There was a distinct relationship between body weight and the onset of death. The tolerance discrepancy between birds and small mammals was atrributed to the fact that the bird's air sacs provided a much enlarged resorption surface in the respiratory tract. Diseases That Mimic Clinical Toxicities

Newcastle disease viruses have been isolated in many South American parrots. Mass casualties among these birds have been observed. Clinically, central nervous system disorders were observed including signs of leg or wing paralysis, torticollis, clonic spasms, and muscular tremors.Z 2 Naturally occurring nutritional secondary hyperparathyroidism occurred in three species of psittacine birds fed sunflower seeds, peanuts, and whole oats. Clinical signs consisted of polydipsia, anorexia, loose stools, regurgitation, weakness, and tetanic seizures. In each bird, parathyroid hypertrophy and osteomalacia were found at necropsy. 39 An aberrant Leucocytozoon infection in budgerigars has been reported. Duration of illness was one to six days. Depression, reduced activity, closed eyes, and hyperpnea were noticed. Postmortem examination revealed a thickened hemorrhagic pericardium. The cardiac muscle was studded with gray nodules. Wild birds, carriers of the disease, were thought to have contaminated foodstuffs eaten by domestic birds.38 Ten Recommendations for the Client to Prevent Poisonings in Pet Birds

1. Feed a broad-spectrum, complete diet as recommended by your veterinarian. 2. Feed only fresh foodstuffs and fresh water. 3. All foods that can be washed should be washed. 4. Do not use insecticides, rodenticides, herbicides, or fungicides in an area to which your pet bird has access. If you must use one of these substances, seek the advice of your veterinarian as to which would be safest and how best to apply the substance. 5. Use drugs only upon recommendation of your veterinarian. 6. Do not smoke around your bird. Make sure any tobacco or cigarette butts are removed from the area before allowing your bird to fly free. 7. Keep your bird away from houseplants. They will appreciate it and he will too! 8. Your bird should always have access to fresh air. Do not leave the bird in a closed room close to a heater or stove unless you believe in the canary-in-the-coal-mine theory. 9. Disinfectants, caustics, cleaners, and solvents should not be used around your bird.

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10. At the first sign of abnormal behavior, call your veterinarian. When bringing a bird to your veterinarian bring him in his cage. Simply empty the water dish. Do not clean the cage! CLINICAL TOXICITIES OF CAGED WILD BIRDS The anachronism of the title of this section is sad but true. We have all been confronted by children and adults who bring orphaned, injured, or sick wild animals to the veterinary clinician. The toxins we release (perhaps unwittingly) into the atmosphere have far-reaching effects. They not only destroy the intended victim but also those who prey on the carcass. It is to those unintended victims we address this section. Admittedly we are treating the symptom, not the cause. Pesticides and Agricultural Poisons We have included some of the common chemicals as representative of a type of pesticide or poison. Many additional pesticides and agricultural poisons are now in wide use. Apparently a widespread decline in populations of birds at the top of the ecological food chain study is underway. These birds live in environments that are subject to many changes, including increasing pollution of all kinds. Pesticides certainly head this list. Certain characteristics of these pesticides such as DDT are causing and have caused concern. The peregrine falcon has only a few breeding places remaining in the United States. Bald eagles are scarce and their reproductive success is exceedingly low. Similar occurrences have been noted in the sparrow hawk, osprey, and golden eagle. Halogenated hydrocarbon insecticides such as DDT are potent stimulators of drug and steroid sex hormone metabolism in mammals and in birds; the breakdown of sex hormones may explain in part the devastating effect of DDT on reproduction in some bird populations.16· 23 The primary use of DDT is as an insecticide. Signs include ataxia, wing drop, jerkiness in gait, continuous whole body tremors,6 falling, and convulsions. Mortalities have occurred from one to two days after single oral administration. Treatment consists of thorough washing with soap if exposure is dermal, saline cathartic via stomach tube if exposure is oral, and control of seizures with barbiturates based on weight of bird (see Table 1). Diagnostically, the highest levels of DDT concentrations were found in the brain and were found to be the best indicators of DDT toxicity. 13 Aroclors or polychlorinated biphenyl (PCB's) are used as industrial plasticizers and heat exchange agents, insulators, and adhesive additives. In birds a depressed growth rate occurs at lower levels of exposure. There is possibly a two to three day transient stasis of the gut. Pericar-

ToxiCITIES

OF

DoMESTIC AND WILD CAGED BIRDS

665

dial and pulmonary edema result in gasping birds. Advanced stages include droopiness, ruffled feathers, weakness, and deaths. Treatment must be symptomatic and supportive. The feeding of charcoal and phenobarbital does not seem to increase the elimination of PCB residues. PCB's are better enzyme inducers than DDT, i.e., they are better inducers of drug metabolizing and sex hormone metabolizing enzymes. Embryonic mortality in several groups of wildfowl have exceeded 50 per cent. 4 It has become clear that pollution of the environment by PCB's is a very serious problem. PCB' s accumulate in food chains as the result of their chemical stability and the fact that they are readily soluble in fats. 37 Actidione or cyclohexamide, a fungicide, caused goose-stepping, ataxia, polydipsia, wing drop or wings crossed high over the back, wing shivers, periodic falling, and prostration in mallards. Signs of intoxication appeared within several hours of treatment and in some survivors took as long as a month to disappear. Necropsies were unrewarding. 36 Chlordane used as an insecticide has caused ataxia, tailup, use of wings for balance, falling, pronation, neck muscle twitching, and tremors. Mortalities occurred in one to eight days with some survivors exhibiting signs for up to four weeks. 36 A herbicide, 2,4-D, caused acute signs of polydipsia, ataxia, tachypnea, tremors, prostration, ptosis of eyelids, and salivation. Gastrointestinal and endocardial hemorrhages were seen on autopsy in mortalities. These signs were seen in numerous birds. 36 DDVP (vapona, dichlorvos) used primarily as an insecticide caused goose-stepping, ataxia, use of wings to aid in balance, tremors, and convulsions. Variou~ internal hemorrhages were found at necropsy in mallards and pheasants. 36 Gophacide, a rodenticide, caused acute signs in numerous birds including the golden eagle. Included signs were myasthenia, arched back, anorexia, ataxia, wings crossed high over the back, salivation, miosis, ptosis of eyelids, dyspnea, tetanic seizures, and opisthotonos. Occasionally, signs did not develop for four days. Survivors took as long as a week to regain normal appearance and behavior.36 Hepatochlor, an insecticide, caused mortalities at night on the sixth and eighth day after ingestion. Signs seen were ataxia, excessive swallowing, and nutation during the day of ingestion. 36 Lindane (gamma BHC), an insecticide, caused regurgitation, polydipsia, tremors, circling, weakness, slowness of reflexes, and opisthotonos in mallards. 36 Malathion, an insecticide, caused ataxia, walking on toes, wing drop, falling stiffly with wings spread, tenesmus, foamy salivation, and tremors. Mortalities in mallards occurred within several hours to 24 hours. 36 Nicotine sulfate (Blackleaf-40- see section on Insecticides, Domes-

666

BERNARD F. FELDMAN, SAMUEL

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tic Caged Birds), an insecticide, caused wing shivers or fasciculations, ataxia, excessive swallowing and chewing motions, masseter tenseness, mild narcosis, and terminal wing beat convulsions or opisthotonos. Mortalities in mallards, pheasants, quail, and pigeons occurred as rapidly as six minutes to as late as two days following treatment. 36 Rotenone, an insecticide, caused acute signs that included ataxia, nutation, dyspnea, polyuria, feathers fluffed or held tightly to body, wing drop, neck pulled in, and immobility. Signs were observed less than an hour after single oral administration. Complete recovery took as long as a week in mallards and pheasants. 36 Sevin, a carbamate insecticide, caused acute signs of ataxia, weakness, salivation, tachypnea, tremors, tetany, paralysis, coma, and convulsions. These signs occurred in numerous avian species. 36 Atropine sulfate should be administered slowly intravenously until the patient shows clinical signs of atropinization (mydriasis and decreased salivation). Atropine may be used cautiously at a dosage of l mg per kg.19 Sodium arsenate, a herbicide and insecticide, had acute toxic effects on mallards. Ataxia, high carriage, and tetanic seizures occurred. Signs persisted five to nine days in survivors. Mortalities usually occurred within 24 hours. 36 Sodium monofluoracetate ("1080"), a mammal control agent, has been shown to have a moderate to high degree of cumulative action in mallards. Body systems affected included respiratory, central nervous, and musculoskeletal. Signs such as dyspnea, ataxia, weakness, tremors, and convulsions were noted. 36 There is no known treatment in birds. Strychnine used in bird and mammal control caused a wide variety of acute signs. Feathers fluffed or held tightly against the body, fasciculation, wing drop, tails pointed down, salivation, tremors, ataxia, hyperacusis, muscle tenseness, recurring convulsions or tetanic seizures, anorexia, tachycardia, immobility, and violent convulsions were included. Birds affected were sparrows, pigeons, and golden eagles. Signs appeared peracutely. Survivor's recovery was generally complete within a few hours except for the eagle which took as long as 48 hours to recover. 36 Pentobarbital in doses sufficient to maintain relaxation is acceptable (see section on Therapeutic Drug Intoxication, Domestic Caged Birds). More prolonged maintenance may be accomplished by inhalation anesthesia or by administration of the muscle relaxant methocarbamol (Robaxin) (67 mg per kg). 26 Glucose may be given intravenously to keep energy levels elevated. Comments on Pesticides

Representative data related to food consumption and body weights of different species and ages of birds are needed. Based on a wide range of body weights and species feeding habits, the smallest birds

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may consume at least 10-fold more food in terms of milligram per kilogram of body weight per day than the largest birds. Considering the variation in pesticide residues on different types of plants as representatives of bird food particles, the daily dietary intake of pesticides by birds (expressed as mg per kg per day) may vary at least 100-fold in environments treated with the same dosage of pesticideP Indeed, elevated insecticide residues in smaller birds may have secondary effects on raptors (birds of prey) feeding upon them. While it is unlikely that signs alone can ever surely identify a toxicant, they sometimes can eliminate certain known toxicants from further consideration. When the development of toxic signs produces a clear-cut pattern, factors such as time of onset, duration, and time of recovery may have implications for the speed and thoroughness of absorption, the rate of metabolism or elimination, and the cumulativeness of residues in the tissues. 36 Lead and Other Inorganic Toxicants

Among the inorganic chemicals, lead has caused the greatest number of poisonings among birds. Waterfowl are especially involved as they seem to mistake lead shot for grit or seeds. Poisoning of North American waterfowl resulting from the ingestion of lead shot by ducks, geese, and swans causes an estimated annual mortality of 2 to 3 per cent of the population. To alleviate this problem the search for a suitable substitute for lead has been underway since the early 1950's. Proposed substitutes for lead shot were evaluated in a series of acute toxicity tests with pen-reared mallards. Most candidate materials were as toxic to ducks as commercial lead shot. Coating or alloying lead with other metals only delayed mortality among dosed ducks. The reputedly "disintegrable" lead shot with a water soluble binder and lead-containing biochemical additives was also as toxic to mallards as commercial lead shot. Mortality was not significantly different among lead-dosed adults or first-year hen and drake pen-reared mallards; lead-dosed adult, wild mallards of both sexes; and lead-dosed adult, male black ducks (Anas rubripes). The ingestion of one lead shot, size 4, by each of 80 pen-reared mallards caused an average mortality rate of 19 per cent. The presence and type of grit in the gizzard had a measurable effect on erosion of ingested shot and on shot retention among dosed mallards. Significantly, fewer lead-dosed ducks died when fed crushed oyster shell grit than either when fed quartz grit or not fed grit. 24 Birds suffering from lead poisoning show lowered food intake, weakness, weight loss, drooping wings, ataxia, inability to fly, and green diarrhea. Lead also affects the nervous system producing paralysis of the extensor muscles of the most frequently used appendage. 6 On necropsy the birds appeared to be emaciated. The gallbladder

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was greatly enlarged and the proventriculus was often impacted, perhaps due to direct stimulation of the smooth muscles due to lead salts, resulting in abnormal contractions. 6 The most pronounced findings in blood were increased red cell fragility, slight anemia, basophilic stippling of the red cells, and an increased number of reticulocytes. In addition, acid-fast inclusion bodies were found in the kidney tubules in mallards and mourning doves. 6 (For treatment see section on Rodenticides and Metals- Clinical Toxicities of Domestic Caged Birds.) Phosphorus poisoning in black ducks and mallards caused depression and terminal convulsions. In the laboratory, white phosphorus (1 to 3 mg per kg) resulted in fatty degeneration of the liver, kidneys, and muscle. Chronic exposures produced blood dyscrasias. 6 Salt poisoning caused signs under laboratory conditions of depression, thirst, tremors, incoordination, coma, and death. Poisonings have occurred following salting of roads in winter. Among others, quail and pheasants were affected. 6 Mercurials used as fungicides (Merna RM) and seed disinfectants (Ceresan L, Ceresan M) caused ataxia, ataraxia, low carriage, hunching up with feathers, wing drop, neck pulled in, blinking, dyspnea, and immobility. Mortalities occurred several days to several weeks post ingestion. Pheasant survivors produced slightly less egg hatchability than did a studied control group. 36 In an experimental feeding of methylmercury to red-tailed hawks, the signs of poisoning prior to death were essentially neurological. Pathologic changes were swelling of axons of myelinated nerves in the· spinal cord and dilation of myelin sheaths and loss of myelin. 9

Biological Toxins Botulism is a disease that results from the ingestion of the toxin of Clostridium botulinum. The toxin is elaborated while the organism is growing as a saprophyte and is one of the most toxic substances known. In a natural outbreak of botulism in pheasants, numerous sick and dying birds were found. The birds manifested a sitting paralysis and when moved uttered a pronounced squawk possibly indicating pain in joints and muscles. The affected birds that were able to move, walked with a stilty gait. Incoordination of wing and leg movement was observed in morbid birds. The affected birds did not display significant head and neck paralysis. The source of the infections was toxic fly larvae found on dead birds. C. botulinum is most ubiquitous and decaying flesh creates an ideal habitat for the anaerobic organism. Fly larvae seem to have the capability of concentrating toxin. When another bird eats the larvae it picks up a lethal dose and the cycle is perpetuated. 10 The best protection is to remove dead birds and decaying plant matter. New fresh feed should

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be given. Water dishes should be washed and feeders disinfected.U Toxoids may be useful in controlling botulism in large aviaries or game farms. 33 Mycotoxicosis (aflatoxin) and blue-green algae toxin (see section on Fungal and Other Food Toxins and Miscellaneous Household Hazards- Clinical Toxicities of Domestic Caged Birds). Oil-soaked birds and their treatment is a major environmental catastrophe faced by veterinarians along the coasts or on any major waterway where petroleum is transported. As this is a specialized subject and has been well documented, the reader is referred to the selected reading list at the end of this article. Several excellent discussions on this subject have been selected and listed. Toxicology of Feral Bird Control Feral birds often create nuisances, are potential hazards around airports and public buildings, and cause crop loss and damage. Of the thousands of bird species only a few are classified as nuisance or pest birds and are not protected by state or federal migratory statutory laws or regulations. In a few cases some of the species may be regarded as nuisance birds in a particular location but are completely protected (gulls, for instance). Other target species include pigeons, starlings, sparrows, blackbirds, cowbirds, grackles, and crows. Numerous substances have been used for control. Diazocholesterol dihydrochloride* has been used as in chemical control of pigeon reproduction and was found to be 100 per cent effective in inhibiting pigeon reproductionP As the substance is administered by coating whole kernel corn, secondary effects are probable. Pheasants, quail, ducks, and geese are grain eaters, are protected species, and could be affected. Sodium ftuoroacetate (" 1080") caused sudden death in pigeons, sparrows, and doves. Invariably secondary deaths in cats, dogs, and foxes were reported when this substance has been broadcast. 25 Signs include respiratory and central nervous system effects such as dyspnea, ataxia, weakness, tremors, and convulsions. Death usually occurs within 24 hours. Alpha chloralose treated whole grain has been used as a stupefying bait for pigeon control. This substance has been used alone or in combination with pentobarbitone sodium or quinalbarbitone sodium. These drugs have general narcotizing results that are quickly followed by death. Some spontaneous recoveries have been reported. Although no apparent secondary effects have been reported, especially in cats, potential secondary hazard does exist. These substances also had an effect on sparrows and other birds. 25 • 35 *Ornitrol, G. D. Searle and Company, Chicago, Illinois.

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The most commonly used substance for feral bird control is 4aminopyridine. * This substance is apparently the most humane product used. It is intended for flock dispersal and is not intended to cause extensive deaths. At doses near the LD 50 , initial effects were noted in 10 to 15 minutes and death occurred in 15 minutes to four hours. Occasionally, the tremor and/or convulsive stages were accompanied by audible vocalizations produced by strong, involuntary contraction of the diaphragm. 29 The first observed change in behavior occurring in one to two seconds was a quick raising of the shoulders accompanied by eye blinking. A second change, ataxia (wobbling, unsteadiness, and leaning in one direction with overcompensation in the other direction), occurred in several minutes. All of these are signs of "alarm" and therefore trigger flock dispersal. External stimuli such as loud noises or touching failed to elicit a response. Vomition occurred occasionally. Convulsions followed these early signs. Terminal events were prostration and hyperventilation. 20 In a recent study, birds killed by ingesting cracked corn baits containing 4-aminopyridine, were fed to dogs, rats, magpies, and three species of hawks. In addition, oral doses were administered. The test animals consumed the equivalent of up to 3.4 LD 50 doses a day for 20 days in repeated feedings. None showed any sign of intoxication or gross abnormalities at necropsy. 30 Clinically we have been presented with affected pigeons. Our treatment has been largely symptomatic-0.25 to 0.5 ml methocarbamol (Robaxin) intramuscularly. It has been our observation that signs of recovery (cessation of nervous signs) will occur within 15 minutes. Most recovering birds will vomit following injection of methocarbamol. Equithesin has also been used with a modicum of success (see section on Therapeutic Drug Intoxication- Clinical Toxicities of Domestic Caged Birds). These treatments have been successful with larger birds (hawks, eagles, and pigeons). With smaller birds (cardinals and sparrows) we have had poor results. The eagles and hawks treated were the suspected results of secondary poisoning, i.e., ingestion of weakened affected birds. This is contrary to the findings cited in the above study. Treatment as outlined was successful. Complete recovery occurred in 24 hours. Though we have not conducted research in specific therapeutics, 4-aminopyridine is a nitrogen compound. Treatment of nitrogen compound poisoning includes gastric lavage, oxygen, and methylene blue (if methemoglobinemia is a problem). Laboratory findings could include an increase in blood methemoglobin as determined photometrically, and reduction in numbers of circulating red blood cells. Hepatic cell function impairment may be indicated by appropriate testing. Normal clinical laboratory values in many species are available.5 • 8 • 27

*Avitrol- Avitrol Corporation, Tulsa, Oklahoma.

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Several interesting points are worth mentioning. Robins are not grain eaters and in our experience have not been affected. Once treated baits are used in an area and cause "alarm," other birds will not eat these baits. In fact, birds will eat around treated baits.

REFERENCES I. Amand, W. B.: Avian Anesthesia. In Kirk, R. W. (ed.): Current Veterinary Therapy V.

Philadelphia, W. B. Saunders Co., 1974, pp. 574-579. 2. Barros, S. S., and Londero, A. T.: Cardiac zygomycoses in an Australian parakeet. Sabouradia, 10:189-190, 1972. 3. Buck, W. B., et al.: Clinical and Diagnostic Veterinary Toxicology. Dubuque, Kendall-Hunt Publishing Co., 1973. 4. Bush, B., et al.: Toxicity and persistence of PCB homologs and isomers in the avian system. Arch. Environ. Contam. Toxicol., 2:195-210, 1974. 5. Coturnix, National Academy of Sciences, Washington, 1969. 6. Davis, J. W., et al.: Infectious and Parasitic Diseases of Wild Birds. Ames, Iowa State University Press, 1971. 7. Ehrsam, H.: Fatal poisoning of small pet birds following accidental overheating of cooking pans lined with polytetrafluorethylene. Schweiz. Arch. Tierheilkd., Ill: 181-186, 1969. 8. Feldman, B. F.: Some laboratory findings in waterfowl affected by an oil spill. Bull. Amer. Soc. Vet. Clin. Pathol., 3:45-50, 1974. 9. Fimreite, M., and Karstad, L.: Effects of dietary methyl mercury on red-tailed hawks. J. Wild!. Mgmt., 35:293-300, 1971. 10. Fish, N. A., et al.: A report on a natural outbreak of botulism in pheasants. Canad. Vet. .J., 8:10-16, 1967. 11. Gamebird Medication Guide. Veterinary Science Extension, Pennsylvania State University, June 8, 1970. 12. Gerlach, H.: Lecture Notes. Davis, University of California, 1970. 13. Greichus, Y. A., and Hannon, M. R.: Distribution and biochemical effects of DDT, DDD and DDE in penned double-crested cormorants. Toxicol. Appl. Pharmol., 26:483-494, 1973.· 14. Gullion, G. W.: Chemical control of pigeon production. Trans. 35th N. Am. Nat. Res. Conf., pp. 47-55, 1970. 15. Hess, R., and Staubli, W.: Mechanism of atherogenesis in the parakeet. Prog. Biochem. Pharmacol., 4:470-473, 1968. 16. Kappas, A., and Alvares, A. P.: How the liver metabolizes foreign substances. Sci. Am., 232:22-31, 1975. 17. Kenaga, E. E.: Factors to be considered in the evaluation of pesticides to birds in their environment. Environ. Qual. Safety, 2:166-181, 1973. 18. Kirk, R. W., and Bistner, S. 1.: Handbook of Veterinary Procedures and Emergency Treatment, 2nd ed. Philadelphia, W. B. Saunders Co., 1975. 19. Kruckenberg, S. M.: Organophosphate and carbamate poisoning. In Kirk, R. W. (ed.): Current Veterinary Therapy V. Philadelphia, W. B. Saunders Co., 1974, pp. 142-143. 20. Kruckenberg, S. M., and Feldman, B. F.: Personal observations, 1975. 21. Lafeber, T. ].: Physical examination, laboratory and medication techniques and hospitalization procedures for the common parakeet and canary. in Kirk, R. S. (ed.): Current Veterinary Therapy V. Philadelphia, W. B. Saunders Co., 1974, pp. 533-543. 22. Leuthgen, W., and Wik, R.: Newcastle disease in recently imported parrots. Deut. Tieraerztl. Wochenschr., 77:407-408, 1970. 23. Longcore, J. R., et al.: Changes ·in mineral composition of eggshells from black ducks and mallards fed DDE in the diet. Bull. Environ. Contam. Toxicol., 6:345-350, 1971. 24. Longcore, J. R., et a!.: Toxicity of lead and proposed substitute shot to mallards. Special Scientific Report-Wildlife No. 183, Washington, 1974.

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25. Morris,]. G.: The control of feral pigeons and sparrows associated with intensive animal production. Aust.]. Sci., 32:9-14, 1969. 26. Osweiler, G. D.: Strychnine poisoning. In Kirk, R. W. (ed.): Current Veterinary Therapy V. Philadelphia, W. B. Saunders Co., 1974, pp. 123-125. 27. Petrak, M. L.: Diseases of Cage and Aviary Birds. Philadelphia, Lea & Febiger, 1969. 28. Rapley, W.: Food requirements of birds. Ann. Proc. Am. Assoc. Zoo Vet., 121-140, 1973. 29. Schafer, E. W., et al.: A summary of acute toxicity of 4-aminopyridine to birds and mammals. Toxicol. Appl. Pharmacal., 26:532-538, 1973. 30. Schafer, E. W., et al.: Hazards with 4-aminopyridine baits.]. Wild!. Mgmt., 38:424426, 1974. 31. Schmael, D., and Osswald, H.: Carcinogenesis in different animal species by diethylnitrosamine. Experentia, 23:497-498, 1967. 32. Seneviratna, P.: Diseases of Poultry Including Cage Birds. Bristol, John Wright and Sons, Ltd., 1969. 33. Shave, H. L.: Progressive pathologic signs of botulism in pheasants.]. Wild!. Dis., 6:402-403, 1970. 34. Stunkard,]. A., and Miller,]. C.: An outline guide to general anesthesia in exotic species. Vet. Med. Sm. Anim. Clin., Sept., 197 4. 35. Thearle. R.]. P.: Improved stupefying baits for the control of town pigeons. Int. Pest. •"ontr., 13:11-14, 16, 19, 1971. 36. Tucker '. K., and Crabtree, D. G.: Handbook of Toxicity of Pesticides in Wildlife. Resm. , .? Publication No. 84, March, 1970. 37. Vos, H. ·.: Toxicology of polychlorinated biphenyls (PCB's) and impurities. Tijdschr. Diergeneesk., 97:1378-1385, 1972. 38. Walker, D., and Garnham, P. C.: Aberrant leucocytozoon infection in parakeets. Vet. Rec., 91:70-72, 1972. 39. Wallach,]. D., and Flieg, G. M.: Nutritional secondary hyperparathyroidism in captive psittacine birds. J.A.V.M.A., 151:880-883, 1967. 40. Zook, B. C., et al.: Lead poisoning in captive wild animals.]. Wild!. Dis., 8:264-273, 1972.

SELECTED READINGS

Aflatoxin and Birds Goldblatt, L. A. (ed.): Aflatoxin, Scientific Background, Control, Implications. Academic Press, New York, 1969. Bacterial Toxins and Birds Creitz, J. R., and Small, N. N. Escherichia coli septicemia in pheasants. Bull. Wild!. Dis. Assoc., 3:68-69, 1967. Gross, W. B., and Smith, L. DS.: Experimental botulism in gallinaceous birds. Avian Dis., 15:716-722, 1971. Holdeman, L. V.: The Ecology and Natural History of Clostridium botulinum. ]. Wild!. Dis., 6:205-210, 1970. Clinical Toxicology and Birds Barkan, B. A., and Oehme, F. W.: A classification of common Midwestern animal toxicoses. Vet. Toxicol. (News from the Am. Coil. Vet. Toxicol.) 17:37-49, 1975. Gestner, H.: Diseases and toxicologic phenomena in psittacine birds-A bibliography. National Library of Medicine, Toxicology Information Response Center, March, 1973. Oiled Birds, Care and Aftercare Harris,]. M.: Treatment of oil soaked birds. In Kirk, R. W. (ed.): Current Veterinary Therapy V. Philadelphia, W. B. Saunders Co., pp. 564-566, 1974. Naviaux,]. L.: Aftercare of oil covered birds. National Wildlife Foundation, Pleasant Hill, California, 1972. Pesticides and the Environment and Birds Bunyan, J. P., et al.: Organophosphorus poisoning: A comparative study of the toxicity of chlorfenvinphos to the pigeon, the pheasant, and the Japanese quail. Pest. Sci., 2: 148-151 ' 1971.

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Bunyan,]. P., et al.: Organophosphorus poisoning: Chronic feeding of some common pesticides to pheasants and pigeons. J. Agric. Food Chern., 17:1027-1032, 1969. Bunyan,]. P., and Taylor, A.: Esterase inhibition in pheasants poisoned by thimet.]. Agric. Food Chern., 14:132-137, 1966. Dahlgren, R. B., and Linder, R. L.: Effects of polychlorinated biphenyls on pheasant reproduction, behavior, and survival.]. Wild!. Mgmt., 35:315-319, 1971. Effects of Pesticides on Fish and Wildlife. United States Department of Interior, Fish and Wildlife Circular 226, 1964. Environmental Health Perspectives. United States Department of Health, Education and Welfare, Volume 9, December, 1974. Gupta, P. K., and Paul, B.S.: Effect of malathion and its toxicity on Gallus domesticus. Indian]. Exp. Bioi., 9:455-457, 1971. Heath, R. G., et al.: Comparative Dietary Toxicities of Pesticides to Birds. Special Scientific Report- Wildlife No. 152, Washington, February, 1971. Hudson, R. H., et al.: Effect of age on sensitivity: Acute oral toxicity of 14 pesticides to mallard ducks of several ages. Toxicol. Appl. Pharmacol., 22:556-561, 1972. Martin, W. E.: Organochlorine insecticide residues in starlings. Pest. Monitor. ]., 3:102-114, 1969. Menzie, C. M.: Metabolism of Pesticides. United States Department of Interior, Special Scientific Report- Wildlife No. 96, Washington, May, 1966. Schafer, E. W.: The acute oral toxicity of 369 pesticidal, pharmaceutical and other chemicals to wild birds. Toxicol. Appl. Pharmacol., 21:315-330, 1972. Sherman, M., et a!.: Comparative toxicity of 4 halogenated organophosphorus insecticides to chicks. Japanese quail and diptera.]. Econ. Ent., 64:814-819, 1971. Sweeny, K. H., et a!.: Development of Field Applied DDT. Office of Resources and Development. United States Environmental Protection Agency, Washington, May, 1974. Tucker, R. K., and Haegele, M.A.: Comparative acute oral toxicity of pesticides to six species of birds. Toxicol. Appl. Pharmacol., 20:57-65, 1971. Tucker, R. K., and Crabtree, D. G.: Handbook of Toxicity of Pesticides to Wildlife. Resource Publication No. 84, Washington, March, 1970. Vos,]. G., et al.: Toxicity of hexachlorobenzine in Japanese quail with special reference to prophyria, liver damage, reproduction, and tissue residues. Toxicol. Appl. Pharmacol., 18:944-957, 1971. Department of Infectious Diseases Veterinary Medical Sciences Building Kansas State University Manhattan, Kansas 66506